Evidence map›Paper›PMID 25923821›Full record

ReviewBritish journal of clinical pharmacology2015

Calcitonin gene-related peptide in the joint: contributions to pain and inflammation.

David A Walsh, Paul I Mapp, Sara Kelly

Open access · bronzeAbstract readReview
In one paragraph

Review in British journal of clinical pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
3.9field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

72 citing papers in PubMed, 128 citations in OpenAlex.

  1. Trial
  2. Article
  3. TRPM2 is a direct pain transducer.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  4. Review
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  16. Observational
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  18. Pain mechanism and management strategy of rheumatoid arthritis.Frontiers in pain research (Lausanne, Switzerland) · 2025
    Review
  19. Article
  20. Article

12 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

David A WalshProfessor of Rheumatology, Director Arthritis Research UK Pain Centre University of Nottingham, Clinical Sciences Building, City Hospital, Hucknall Road, Nottingham, NG5 1PB.
Paul I MappResearch Fellow, Arthritis UK Pain Centre, University of Nottingham, NG5 1PB.
Sara KellyAssistant Professor in Neuroscience, School of Biosciences, University of Nottingham, Sutton Bonnington Campus, Nr Loughborough, Leicestershire, LE12 5RD, United Kingdom.
University of Nottingham · GB

Funding

Arthritis Research UK 18769
6 · The paper itself

Abstract

Arthritis is the commonest cause of disabling chronic pain, and both osteoarthritis (OA) and rheumatoid arthritis (RA) remain major burdens on both individuals and society. Peripheral release of calcitonin gene-related peptide (CGRP) contributes to the vasodilation of acute neurogenic inflammation. Contributions of CGRP to the pain and inflammation of chronic arthritis, however, are only recently being elucidated. Animal models of arthritis are revealing the molecular and pathophysiological events that accompany and lead to progression of both arthritis and pain. Peripheral actions of CGRP in the joint might contribute to both inflammation and joint afferent sensitization. CGRP and its specific receptors are expressed in joint afferents and up-regulated following arthritis induction. Peripheral CGRP release results in activation of synovial vascular cells, through which acute vasodilatation is followed by endothelial cell proliferation and angiogenesis, key features of chronic inflammation. Local administration of CGRP to the knee also increases mechanosensitivity of joint afferents, mimicking peripheral sensitization seen in arthritic joints. Increased mechanosensitivity in OA knees and pain behaviour can be reduced by peripherally acting CGRP receptor antagonists. Effects of CGRP pathway blockade on arthritic joint afferents, but not in normal joints, suggest contributions to sensitization rather than normal joint nociception. CGRP therefore might make key contributions to the transition from normal to persistent synovitis, and the progression from nociception to sensitization. Targeting CGRP or its receptors within joint tissues to prevent these undesirable transitions during early arthritis, or suppress them in established disease, might prevent persistent inflammation and relieve arthritis pain.

Indexed as

AnimalsCalcitonin Gene-Related PeptideCalcitonin Gene-Related Peptide Receptor AntagonistsDisease Models, AnimalEndothelial CellsHumansInflammationJointsModels, BiologicalNeovascularization, PathologicPainCalcitonin Gene-Related PeptideCalcitonin Gene-Related Peptide Receptor AntagonistsCalcitonin gene-related peptideinflammationjointspain

Identifiers

PMID25923821
PMCPMC4631170
OpenAlexW1972701083

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.